Scorpion Envenomation 

Updated: Nov 09, 2018
Author: David Cheng, MD; Chief Editor: Joe Alcock, MD, MS 

Overview

Background

Scorpion stings are a major public health problem in many underdeveloped tropical and subtropical countries, especially Sahelian Africa, South India, the Middle East, Mexico, and South Latin America.[1, 2] The estimated annual number of scorpion stings is 1.2 million leading to 3250 deaths (0.27%).[3] For every person killed by a venomous snake, 10 are killed by a venomous scorpion. In Mexico, 1000 deaths from scorpion stings occur per year. In the United States, only 4 deaths in 11 years have occurred as a result of scorpion stings. Furthermore, scorpions can be found outside their normal range of distribution, that is when they crawl into luggage, boxes, containers, or shoes and are unwittingly transported home via human travelers.

A scorpion has a flattened elongated body and can easily hide in cracks. It has 4 pairs of legs, a pair of claws, and a segmented tail that has a venomous spike at the end. Scorpions vary in size from 1-20 cm in length.


Centruroides limbatus, identified by Scott Stockw Centruroides limbatus, identified by Scott Stockwell, PhD. A small barb at the base of the stinger may be helpful in identifying Centruroides or Tityus species, although its presence is variable. Photo by Sean Bush, MD.

See Arthropod Envenomation: From Benign Bites to Serious Stings, a Critical Images slideshow, for help identifying and treating various envenomations.

Out of 1500 scorpion species, 50 are dangerous to humans. Scorpion stings cause a wide range of conditions, from severe local skin reactions to neurologic, respiratory, and cardiovascular collapse. Envenomation from most scorpions results in a simple, painful, local reaction that can be treated with analgesics, antihistamines, and symptomatic/supportive care. This article focuses on scorpions that generally are considered more dangerous to humans.

Almost all of these lethal scorpions, except the Hemiscorpius species, belong to the scorpion family called the Buthidae. The Buthidae family is characterized by a triangular-shaped sternum, as opposed to the pentagonal-shaped sternum found in the other 5 scorpion families.

Scorpions from the family Buthidae (which includes Scorpions from the family Buthidae (which includes almost all of the potentially lethal scorpions) generally can be identified by the triangular sternal plate. In other families of scorpions, this feature is more square or pentagonal. Photo by Sean Bush, MD.

In addition to the triangular-shaped sternum, venomous scorpions also tend to have weak-looking pincers, thin bodies, and thick tails, as opposed to the strong heavy pincers, thick bodies, and thin tails seen in nonlethal scorpions.


Centruroides species. Note the slender pincers ge Centruroides species. Note the slender pincers generally characteristic of scorpions from the family Buthidae. Photo by Sean Bush, MD.

The lethal members of the Buthidae family include the genera of Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus, and Centruroides. The following lethal scorpions are found generally in the given distribution:

  • Buthus - Mediterranean area, from Spain to the Middle East

  • Parabuthus - Western and Southern Africa

  • Mesobuthus – Throughout Asia

  • Parabuthus - Western and southern Africa

  • Buthotus (ie, Hottentotta) - Across southern Africa to southeast Asia

  • Tityus - Central America, South America, and the Caribbean

  • Leiurus - Northern Africa and the Middle East

  • Androctonus - Northern Africa to Southeast Asia

  • Centruroides - Southern United States, Mexico, Central America, and the Caribbean (Centruroides exilicauda is found in the Baja California peninsula of Mexico and Centruroides sculpturatus is found in the state of Sonora, Mexico and the southwestern United States, primarily Arizona and small parts of Utah, New Mexico, Nevada, and California.) The accepted taxonomy of the bark scorpion has changed over time. Either C exilicauda or C sculpturatus have been accepted at various times. However, recent evidence from biochemical, genetic, and physiologic characterization of their venom suggests that they are two different species as listed above.

However, these scorpions may be found outside their natural habitat range of distribution when inadvertently transported with luggage and cargo.

In general, scorpions are not aggressive. They are ambush predators, often hiding and waiting for their prey. Scorpions are nocturnal creatures; they hunt during the night and hide in crevices and burrows during the day to avoid the light. Thus, accidental human stinging occurs when scorpions are touched while in their hiding places, with most of the stings occurring on the hands and feet.

Pathophysiology

Scorpions use their pincers to grasp their prey; then, they arch their tail over their body to drive their stinger into the prey to inject their venom, sometimes more than once. The scorpion can voluntarily regulate how much venom to inject with each sting. The striated muscles in the stinger allow regulation of the amount of venom ejected, which is usually 0.1-0.6 mg. If the entire supply of venom is used, several days must elapse before the supply is replenished. Furthermore, scorpions with large venom sacs, such as the Parabuthus species, can even squirt their venom.

The venom glands are located on the tail lateral to the tip of the stinger and are composed of 2 types of tall columnar cells. One type produces the toxins, while the other produces mucus. The potency of the venom varies with the species, with some producing only a mild flu and others producing death within an hour. In addition, there is species variability in venom volume, flow rate, and duration.[4] Generally, the venom is distributed rapidly into the tissue if it is deposited into a venous structure. Venom deposited via the intravenous route can cause symptoms only 4-7 minutes after the injection, with a peak tissue concentration in 30 minutes and an overall toxin elimination half-life of 4.2-13.4 hours through the urine. The more rapidly the venom enters the bloodstream, the higher the venom concentration in the blood and the more rapid the onset of systemic symptoms.

Scorpion venom is a water-soluble, antigenic, heterogenous mixture, as demonstrated on electrophoresis studies. This heterogeneity accounts for the variable patient reactions to the scorpion sting. However, the closer the phylogenetic relationship between the scorpions, the more similar the immunological properties. Furthermore, the various constituents of the venom may act directly or indirectly and individually or synergistically to manifest their effects. In addition, differences in the amino acid sequence of each toxin account for their differences in the function and immunology. Thus, any modifications of the amino acid sequence result in modification of the function and immunology of the toxin.

Scorpion venom may contain multiple toxins and other compounds. The venom is composed of varying concentrations of neurotoxin, cardiotoxin, nephrotoxin, hemolytic toxin, phosphodiesterases, phospholipases, hyaluronidases, glycosaminoglycans, histamine, serotonin, tryptophan, and cytokine releasers. The most important clinical effects of envenomation are neuromuscular, neuroautonomic, or local tissue effects. The primary targets of scorpion venom are voltage-dependent ion channels, of which sodium channels are the best studied. Venom toxins alter these channels, leading to prolonged neuronal activity. Many end-organ effects are secondary to this excessive excitation. Autonomic excitation leads to cardiopulmonary effects observed after some scorpion envenomations. Somatic and cranial nerve hyperactivity results from neuromuscular overstimulation. Additionally, serotonin may be found in scorpion venom and is thought to contribute to the pain associated with scorpion envenomation.

The most potent toxin is the neurotoxin, of which two classes exist. Both types of neurotoxin are heat-stable, have low molecular weight, and are responsible for causing cell impairment in nerves, muscles, and the heart by altering ion channel permeability.

The long-chain polypeptide neurotoxin causes stabilization of voltage-dependent sodium channels in the open position, leading to continuous, prolonged, repetitive firing of the somatic, sympathetic, and parasympathetic neurons. This repetitive firing results in autonomic and neuromuscular overexcitation symptoms, and it prevents normal nerve impulse transmissions. Furthermore, it results in release of excessive neurotransmitters such as epinephrine, norepinephrine, acetylcholine, glutamate, and aspartate. Meanwhile, the short polypeptide neurotoxin blocks the potassium channels.

The binding of these neurotoxins to the host is reversible, but different neurotoxins have different affinities. The stability of the neurotoxin is due to the 4 disulfide bridges that fold the neurotoxin into a very compact 3-dimensional structure, thus making it resistant to pH and temperature changes. However, reagents that can break the disulfide bridges can inactivate this toxin by causing it to unfold. Also, the antigenicity of this toxin is dependent on the length and number of exposed regions that are sticking out of the 3-dimensional structure.

Etiology

The causes of scorpion envenomation are primarily accidental. Scorpions are shy creatures and only sting if threatened, cornered, or disturbed (eg, being sat or stepped upon). Curious individuals are at risk because of increased interaction with the scorpion.

The median lethal dose 50 (LD50) of various scorpion venoms in mg/kg of a subcutaneous injection into mice and the territorial distribution are listed below (unfortunately, humans are much more sensitive than mice):

  • Leiurus quinquestriatus (Middle East) - 0.25 mg/kg

  • Androctonus crassicauda (Saudi Arabia) - 0.08-0.5 mg/kg

  • Centruroides noxius (Mexico) - 0.26 mg/kg

  • Androctonus mauritanicus (North Africa) - 0.32 mg/kg

  • Centruroides santa maria (Central America) - 0.39 mg/kg

  • Tityus serrulatus (Brazil) - 0.43 mg/kg

  • Buthus occitanus (North Africa) - 0.9 mg/kg

  • Centruroides sculpturatus (Southwest United States) - 1.12 mg/kg

  • Mesobuthus eupeus (Iran) - 1.45 mg/kg

Generally, most lethal scorpions have an LD50 below 1.5 mg/kg.

The average yield per scorpion via electrical excitation of the venom gland for a few species is listed below:

  • Tityus species - 0.39-0.62 mg

  • L quinquestriatus - 0.62 mg

  • Buthus species - 0.38-1.5 mg

  • Milking the venom gland produces approximately a 4-fold increase in yield amount compared to electrical excitation.

Epidemiology

Frequency

United States

Approximately 16,000 stings have been reported, with the majority being from the nonlethal scorpions. Only 1 of 30 scorpion species found in the United States is dangerous to humans. The neurotoxin-bearing and potentially lethal scorpion species in the United States is the Arizona bark scorpion in the genus Centruroides.[5] Less than 1% of stings from Centruroides are lethal to adults; however, 25% of children younger than 5 years who are stung die if not treated. The epidemiological features of a patient who has been envenomed show a disposition for rural areas (59.6-73%), with most of the stings occurring in the summer months between 6:00 pm and 12:00 am (49%) and a second peak from 6:00 am to 12:00 pm (30%). Both of these peaks coincide maximum human activity with maximum scorpion activity. In addition, nocturnal envenomations are slightly more common than diurnal, as the scorpion is more active at night. Furthermore, the larger the scorpion population, the larger the incidence rate. Because the offending scorpion is recovered for identification in only 30% of the cases, local knowledge of the type of scorpion populating the area is useful.

The 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS) reported 13,670 case mentions for scorpion envenomations, with 22 "major" outcomes and 0 deaths.[6] However, because of underreporting, this is probably an underestimation of the true number of stings.

International

Scorpion stings occur in temperate and tropical regions, especially between the latitudes of 50°N and 50°S of the equator. Furthermore, stings predominantly occur during the summer and evening times.[1] In addition, the majority of patients are stung outside their home.

Accurate statistics on scorpion envenomation are not available. Many potentially dangerous scorpions inhabit the underdeveloped or developing world. Consequently, numerous envenomations go unreported, and true incidence is unknown. However, it has been estimated that there are 1.2 million scorpion stings per year.[3]

A 5-year surveillance study in Saudi Arabia found 6465 scorpion sting cases with a mean patient age of 23 years, a male-to-female ratio of 1.9, and a higher incidence of stings in the months of May through October.[7]

In Khuzestan province of Iran, 12,150 annual cases occurred, with nocturnal envenomations occurring 60.9% of the time, 39.3% stings occurring on the hands, and 37.3% stings occurring on the feet. June was the highest month for stings, at 16%, and February, the lowest at 0.6%.[8]

Race

No racial predilection exists.

Sex

Females may be more susceptible than males to the same amount of scorpion venom because of their lower body weight.

Age

Adults, especially those of workforce age, are stung more often than children. However, children are more likely to develop a more rapid progression of symptoms after a scorpion sting, with increased severity and higher mortality because of their lower body weight,[9] with a global rate of 10 deaths per 1000 cases in children.[10, 11] Furthermore, elderly persons are more susceptible to stings because of their decreased physiologic reserves and increased debilitation.

Mortality/Morbidity

Accurate worldwide data are not available. Scorpion stings are underreported because many envenomations occur in sparsely populated areas with little public health and medical infrastructure. Furthermore, reporting is generally not required.

Most deaths occur during the first 24 hours after the sting and are secondary to respiratory or cardiovascular failure.

The highest reported mortality rate is recorded in data from Mexico, with estimates as high as 1000 deaths in 1 year. In the United States, 4 deaths were reported in an 11-year period according to one source.[12] However, no deaths were reported to the American Association of Poison Control Centers from 1983 to 1999. Only one death from the Arizona bark scorpion (C sculpturatus) has been reported since 1964.[13]

Children and elderly persons are at the greatest risk for morbidity and mortality. A smaller child, a lower body weight, and a larger ratio of venom to body weight lead to a more severe reaction. A mortality rate of 20% is reported in untreated babies, 10% in untreated school-aged children, and 1% in untreated adults, but these rates vary across years and regions.

In terms of venom lethality, the venom of Androctonus australis and Leiurus quinquestriatus are the most toxic. C sculpturatus venom is low in toxicity compared with most scorpions of medical importance.

Furthermore, patients in rural areas tend to fare worse than patients in urban areas because of the delay in getting medical help due to a longer travel time to medical centers and the lack of advanced medical treatments.[14] Fortunately, better public education, improved control of the scorpion population, increased supportive therapies, more technologically advanced intensive care units and advances in immunotherapy have combined to produce a substantial decrease in mortality from these envenomations.[15]

Prognosis

Prognosis is dependent on many factors, including species of scorpion, patient health, and access to medical care. Most patients recover fully after scorpion envenomation.

Symptoms generally persist for 10-48 hours. If the victim survives the first few hours without severe cardiorespiratory or neurologic symptoms, the prognosis is usually good. Furthermore, surviving the first 24 hours after a scorpion sting also carries a good prognosis.

A worse prognosis can be expected with the presence of systemic symptoms such as cardiovascular collapse, respiratory failure, seizures, and coma. Specifically, the following were associated with poor outcomes: Glasgow Coma Score less than 8 (odds ratio [OR], 9.87) and pulmonary edema (OR, 8.46).[16]

In children, the following factors were associated with a higher mortality: metabolic acidosis, tachypnea, myocarditis, pulmonary edema, encephalopathy, and priapism.[17]

Patient Education

Educate all patients about methods to avoid scorpions (see Prevention). Delays in seeking medical treatment are associated with higher likelihood of mortality in children and adolescents.[18]

 

Presentation

History

For patients presenting with scorpion stings, ascertaining the following is essential:

  • Time of envenomation

  • Nature of the incident

  • Description of the scorpion: Specimen identification by an entomologist may be helpful (if the scorpion can be captured safely).

  • Local and systemic symptoms: Pain and paresthesias often are present. Nausea and vomiting are common.

The toxicity, variation, and duration of the symptoms depends on the following factors:

  • Scorpion species

  • Scorpion age, size, and nutritional status

  • Healthiness of the scorpion's stinging apparatus (telson)

  • Number of stings and quantity of venom injected

  • Depth of the sting penetration

  • Composition of the venom

  • Site of envenomation: Closer proximity of the sting to the head and torso results in quicker venom absorption into the central circulation and a quicker onset of symptoms.

  • Age of the victim, as children are more susceptible to severe clinical manifestations

  • Health of the victim

  • Weight of the victim relative to amount of venom

  • Presence of comorbidities

  • Treatment effectiveness

Nonlethal scorpion species tend to produce local reactions similar to a hymenopteran sting, while lethal scorpion species tend to produce systemic symptoms. The duration to progress to systemic symptoms ranges from 5 minutes to 4 hours after the sting. The symptoms generally persist for 10-48 hours.

Physical Examination

Clinical manifestations range from minor local tenderness to multisystem failure followed by death.[19]

Local tissue effects vary among species. Minimal local tissue effects are present with Centruroides envenomation. Significant local tissue reaction rules out C exilicauda envenomation. Tapping over the injury site (ie, tap test) may cause severe pain after a sting by C exilicauda.

Tachycardia and other dysrhythmias are caused by autonomic effects primarily, although direct myocardial toxicity with arrhythmogenic effects has been described.

Hypertension or hypotension may be present.

The patient may have hyperthermia.

Respiratory arrest and loss of protective airway reflexes are common causes of mortality. Pulmonary edema has been described and may be secondary to cardiogenic causes and to increased capillary permeability.

Autonomic effects include the following:

  • Sympathetic overdrive symptoms predominate, causing tachycardia, hypertension, hyperthermia, and pulmonary edema.

  • Parasympathetic symptoms include hypotension, bradycardia, salivation, lacrimation, urination, defecation, and gastric emptying.

Cranial nerve effects include the following:

  • Classic roving or rotary eye movements, blurred vision, tongue fasciculations, and loss of pharyngeal muscle control may be observed.

  • Difficulty swallowing combined with excessive salivary secretions may lead to respiratory difficulty.

Somatic effects include the following:

  • Restlessness and involuntary muscle jerking that can be mistaken for seizures have been described.

  • Presence of true seizures in Centruroides envenomation is controversial and has not been proven to occur. Seizures are described in association with other scorpion envenomations.

Cerebral infarction, cerebral thrombosis, and acute hypertensive encephalopathy have been described with a variety of Buthidae scorpion envenomations.

The signs of the envenomation are determined by the scorpion species, venom composition, and the victim's physiological reaction to the venom. The signs occur within a few minutes after the sting and usually progress to a maximum severity within 5 hours. The signs last for 24-72 hours and do not have an apparent sequence. Thus, predicting the evolution of signs over time is difficult. Furthermore, a false recovery followed by a total relapse is common.

A person who has been stung by a scorpion usually has four signs, with the most common being mydriasis, nystagmus, hypersalivation, dysphagia, and restlessness. The mode of death is usually via respiratory failure secondary to anaphylaxis, bronchoconstriction, bronchorrhea, pharyngeal secretions, and/or diaphragmatic paralysis, even though venom-induced multiorgan failure may play a large role. Death can occur from toxicity or from anaphylaxis. These are two separate things, and many “nonlethal” species can cause anaphylaxis.

Children present with the same symptoms and signs as adults, except their symptoms are more severe and protracted. Furthermore, they may display a restlessness that is out of proportion when compared to any other disease. A child's symptoms have been described as inconsolable crying; uncontrollable jerking of the extremities; and chaotic thrashing, flailing, and writhing combined with contorted facial grimaces. The symptoms mimic a centrally mediated seizure, but the patient is awake and alert the entire time.

The grading of these scorpion envenomations depends on whether or not neurological signs predominate and is as follows:

Nonneurological predominance is graded as follows[2] :

  • Mild - Local signs of erythema, swelling and tenderness (estimated 68.6%)

  • Moderate - Ascending local signs or mild systemic signs (estimated 26.8%)

  • Severe - Life-threatening systemic signs (estimated 4.6%)

Neurologic predominance is graded as follows:

  • Grade I - Local pain or paresthesia at the sting site (83%)

  • Grade II - Pain or paresthesia that has traveled from the sting site (9.1%)

  • Grade III - Either cranial nerve or somatic neuromuscular dysfunction (4.7%)

  • Grade IV - Both cranial nerve and somatic neuromuscular dysfunction (3%)

Local signs

Neurotoxic local effects

Local evidence of a sting may be minimal or absent in as many as 50% of cases of neurotoxic scorpion stings. In fact, tissue necrosis is rarely found.

A sharp burning pain sensation at the sting site, followed by pruritus, erythema, local tissue swelling, and ascending hyperesthesia, may be reported. This paresthesia feels like an electric current, persists for several weeks, and is the last symptom to resolve before the victim recovers.

The tap test is administered by tapping at the sting site. A positive result is when the paresthesia worsens with the tapping because the site is hypersensitive to touch and temperature. In fact, wearing clothing over the area and sudden changes in temperature exacerbate the symptoms. Tapping over the injury site (ie, tap test) may cause severe pain after a sting by C exilicauda.

Cytotoxic local effects

A macule or papule appears initially at the sting site, occurring within the first hour of the sting.

The diameter of the lesion is dependent on the quantity of venom injected.

The lesion progresses to a purpuric plague that will necrose and ulcerate.

Lymphangitis results from the transfer of the venom through the lymphatic vessels.

Nonlethal local effects

Pain, erythema, induration, and wheal may be present.

These are secondary to venom activation of kinins and slow-releasing substances.

Local tissue effects vary among species. Minimal local tissue effects are present with Centruroides envenomation. Significant local tissue reaction rules out C exilicauda (C sculpturatus) envenomation.

Neurologic signs

Most of the symptoms are due to either the release of catecholamines from the adrenal glands (sympathetic nerves) or the release of acetylcholine from postganglionic parasympathetic neurons. One study by Freire-Maia et al (1974) found that the adrenergic signs occur at a low venom dose, while cholinergic signs occur at high venom dose concentrations (ie, >40 mcg/100 g in Tityus serrulatus scorpion venom).[20] Furthermore, the adrenergic phase tended to be more dependent on the venom dose than the cholinergic phase. However, dual manifestations of the adrenergic and cholinergic signs are possible because of varying organ system sensitivities to these neurotransmitters.

Central nervous system signs are as follows:

  • Thalamus-induced systemic paresthesia occurs in all 4 limbs.

  • Patients experience venom-induced cerebral thrombosis strokes.

  • The level of consciousness is altered, especially with restlessness, confusion, or delirium.

  • Patients have abnormal behavior.

  • Ataxia is also a sign.

Autonomic nervous system signs include predominately sympathetic signs, parasympathetic signs, or a combination of signs.

Sympathetic signs are as follows:

  • Hyperthermia

  • Tachypnea

  • Tachycardia

  • Hypertension

  • Arrhythmia

  • Hyperkinetic pulmonary edema

  • Hyperglycemia

  • Diaphoresis

  • Piloerection

  • Restlessness and apprehension

  • Hyperexcitability and convulsions

Parasympathetic signs are as follows:

  • Bronchoconstriction

  • Bradycardia

  • Hypotension

  • Salivation, lacrimation, urination, diarrhea, and gastric emesis (SLUDGE)

  • Rhinorrhea and bronchorrhea

  • Goose pimple skin

  • Loss of bowel and bladder control

  • Priapism

  • Dysphagia

  • Miosis

  • Generalized weakness

Somatic signs are as follows:

  • Rigid spastic muscle of the limbs and torso

  • Involuntary muscle spasm, twitching, clonus, and contractures

  • Alternating opisthotonos and opisthotonus from inactivation of sodium channels, leading to increased sodium and calcium uptake

  • Increased tendon reflexes, especially prolongation of the relaxation phase

  • Piloerection accompanied by goose pimples

Cranial nerve signs are as follows:

  • Classic rotary eye movement may result in ptosis, nystagmus, and blurred vision.

  • Mydriasis is a sign.

  • Patients may have tongue fasciculations.

  • Dysphagia, dysarthria, and stridor occur secondary to pharyngeal reflex loss or muscle spasm.

  • Patients may present with excessive salivation and drooling.

Peripheral nervous system signs include intense local burning pain with minimal swelling at sting site, followed by ascending numbness and tingling, then paralysis and convulsions.

Nonneurologic systemic signs

Cardiovascular signs usually follow a pattern of a hyperdynamic phase followed by a hypodynamic phase. Hypertension is described as follows:

  • Hypotension - Less common and occurs secondary to excess acetylcholine or catecholamine depletion

  • High enough to produce hypertensive encephalopathy

  • Lasts a few hours

  • Observed as early as within 4 minutes after the sting

  • Secondary to catecholamine and renin stimulation

Tachycardia is greater than 130 beats per minute, although bradycardia can be observed.

Transient apical pansystolic murmur is consistent with papillary muscle damage.

Cardiovascular collapse occurs secondary to toxin induced myocarditis biventricular dysfunction and profuse loss of fluids from sweating, vomiting, diarrhea, and hypersalivation. Note the following:

  • Observed in 7-38% of cardiovascular cases

  • Mild envenomation - Vascular effect with vasoconstriction hypertension

  • Moderate envenomation - Left ventricular failure hypotension with and without an elevated pulmonary artery wedge pressure, depending on fluid status of the patient

  • Severe envenomation - Biventricular cardiogenic shock

  • Cardiac dysfunctions attributed to catecholamine-induced myocarditis and increases in myocardial metabolism oxygen demand (leading to myocardial ischemia–induced myocardial hypoperfusion) as well as to the direct effects of the toxin (leading to myocarditis and myocardial conduction interference)[21]

Respiratory signs are as follows:

  • Tachypnea may be present.

  • Pulmonary edema with hemoptysis and a normal-sized heart is observed in 7-32% of respiratory cases. This is secondary to a direct toxin-induced increased pulmonary vessel permeability effect and is also secondary to catecholamine-induced effects of hypoxia and intracellular calcium accumulation, which leads to a decrease in left ventricular compliance with resultant ventricular dilation and diastolic dysfunction.[22]

  • Respiratory failure may occur secondary to diaphragm paralysis, alveolar hypoventilation, and bronchorrhea.

Allergic signs are as follows:

  • Patients may have urticaria.

  • Angioedema is reported.

  • Patients may present with bronchospasm.

  • Anaphylaxis is possible.

Gastrointestinal signs are as follows:

  • Patients may present with excessive salivation.

  • Dysphagia is possible.

  • Nausea and vomiting are reported.

  • Gastric hyperdistention occurs secondary to vagal stimulation.

  • Increased gastric acid output may lead to gastric ulcers.

  • Acute pancreatitis may lead to hyperglycemia.

  • Liver glycogenolysis may occur from catecholamine stimulation.

  • Toxic hepatitis

Genitourinary signs are as follows:

  • Patients have decreased renal plasma flow.

  • Toxin-induced acute tubular necrosis renal failure may occur.

  • Rhabdomyolysis renal failure may result from venom-induced excessive motor activity.

  • Priapism may occur secondary to cholinergic stimulation. One small study by Bawaskar (1982) found a positive prognostic correlation to the development of cardiac manifestations following scorpion stings.[23]

Hematological signs are as follows:

  • Platelet aggregation may occur because of catecholamine stimulation.

  • Disseminated intravascular coagulation with massive hemorrhage may result from venom-induced defibrination.

Metabolic signs are as follows:

  • Hyperglycemia may occur from catecholamine-induced hepatic glycogenolysis, pancreatitis, and insulin inhibition.

  • Increased lactic acidosis may occur from hypoxia and venom-induced increased lactase dehydrogenase activity.

  • Patients may have an electrolyte imbalance and dehydration from hypersalivation, vomiting, diaphoresis, and diarrhea.

Pregnancy complication signs include toxin-induced uterine contraction, eclampsia, but the majority of pregnant females do not experience severe sequela.[24]

Symptoms predictive of hospital admission are as follows:

  • Priapism (odds ratio 150.59)

  • Vomiting (odds ratio 15.82)

  • Systolic blood pressure (SBP) greater than 160 (odds ratio 13.38)

  • Temperature greater than 38ºC (odds ratio 3.66)

  • Heart rate greater than 100 beats per minute (odds ratio 3.35)

Symptomology of specific scorpion species

See the list below:

  • Mesobuthus, Tityus, and Leiurus - Tend to cause severe cardiovascular symptoms

  • Centruroides - Tend to cause neurological symptoms

  • Hemiscorpius - Tend to cause tissue necrosis

Complications

Complications of scorpion envenomation may include the following:

  • Cellulitis and abscess formation at sting site[25]

  • Dilated cardiomyopathy[26, 27]

  • Ankylosis of small joints if the sting occurs at a joint

  • Rhabdomyolysis

  • Persistent paresthesia

  • Antivenin anaphylaxis and serum sickness[28]

  • Iatrogenic, high-dose, sedative-hypnotic respiratory arrest

  • Respiratory arrest

  • Cardiac arrest

  • Shock

  • Seizures

  • Rhabdomyolysis

  • Death

  • Defibrination after M tamulus stings

  • Hemolysis after H lepturus stings

  • Pancreatitis after T trinitatis stings

  • Antivenom-associated reactions

  • Renal failure

 

DDx

 

Workup

Laboratory Studies

Scorpion envenomation cases vary from those requiring no laboratory tests to scenarios requiring extensive hematologic, electrolyte, and respiratory analysis.

Obtain a CBC count, as Hemiscorpius lepturus has been shown to cause severe hemolysis. In addition, marked leukocytosis suggests induction of a venom-mediated systemic inflammatory response‒like syndrome.

Electrolyte evaluation is warranted in patients with venom-induced salivation, vomiting, and diarrhea.

Coagulation parameters should be measured for venom-induced defibrination because, at high concentrations, the venom is an anticoagulant. Defibrination syndrome has been reported following Mesobuthus tamulus stings.

Glucose levels should be measured to evaluate for hyperglycemia from liver and pancreas dysfunction.

Troponin and NT-proBNP elevation suggests myocarditis.

Creatine kinase and urinalysis help evaluate for venom-induced excessive motor rhabdomyolysis. Renal failure may occur secondary to hemoglobinuria from hemolysis (after H lepturus sting) or myoglobinuria from rhabdomyolysis

Obtain amylase/lipase values to assess for pancreatitis, which is common, from Tityus trinitatis stings.

Patients may have increased aspartate aminotransferase and alanine aminotransferase levels from venom-induced liver cell destruction.

Increased catecholamine, aldosterone, renin angiotensin, and antidiuretic hormone levels are detected a few hours after the sting. The increased levels persist for 6 hours, after which a gradual decline occurs.

Obtain arterial blood gas (ABG) measurements as indicated for respiratory distress or to determine acid/base status.

Additional laboratory abnormalities that may have research relevance include interleukin (IL)–1 levels, which have been reported to be elevated.

High levels of IL-6, interferon-gamma, and granulocyte-macrophage colony-stimulating factor are reported in severe envenomations.

Radiolabeled antibodies or immunoenzymatic assays help quantify the serum venom level because an association exists between the clinical signs of envenomation and this level.[29]  However, it is rarely used, owing to cost and because clinical grading is as effective. It is most likely only used as a research tool.

Imaging Studies

Obtain a chest radiograph in cases of respiratory difficulty. Unilateral pulmonary edema may be seen on chest x-ray films because of the venom effect on pulmonary vascular permeability.

Echocardiography is more sensitive than electrocardiography and creatine kinase assays for assessing myocardial compromise after a scorpion sting. Findings show a diffuse global biventricular hypokinesis with a decreased left and right ventricular ejection fraction of approximately 0.14-0.38. This dysfunction can appear just a few hours after the sting and usually normalizes within 4-8 days. Serial echocardiography findings show that the return of left ventricular function to a normal state correlates to clinical cardiorespiratory improvement.

Color-flow Doppler study findings show mitral incompetence, probably secondary to venom-induced dilated cardiomyopathy.

Myocardial perfusion scintigraphy can also be used to investigate the contractility and perfusion of the cardiac tissue.[30]

Other Tests

Arterial blood gas determinations show a decrease in arterial oxygenation tension and an increase in PCO2 within 15 minutes of the envenomation, findings consistent with mild metabolic acidosis.

Pulmonary artery catheterization findings may include the following:

  • Elevated systemic vascular resistance occurs up to 4 times the normal level, with elevated mean arterial pressure (MAP) of 203 mm Hg.

  • Left ventricular failure produces a MAP of 57-69 mm Hg.

  • Biventricular failure produces a MAP of 47 mm Hg.

  • Low cardiac index occurs with elevated filling pressures.

Perform serial spirometry measurements to help detect impending venom-induced diaphragmatic failure.

Electrocardiography, if indicated, should be performed. ECG changes persist for 10-12 days before normalizing. ECG changes are observed in 63% of children who have been envenomated. Rhythm disturbances are not dose-dependent but are related to the venom composition. Note the following:

  • First-degree block - 10.2%

  • Bundle-branch block - 12.8%

  • Ventricular repolarization abnormalities - 15%

  • T-wave inversion - 39%

  • ST changes - 39%

  • QTc prolongation - 53%

  • Sinus tachycardia - Most common rhythm

  • A possible sequence of ECG changes has been noted. This sequence starts with bizarre, broad-notched, biphasic, peaked T waves with a beat-to-beat variation. This bizarre T wave is followed by the appearance of tiny Q waves and then atrioventricular dissociation with an accelerated junctional rhythm.

Procedures

Cerebrospinal fluid pleocytosis is evident on spinal tap studies.

Histologic Findings

The local sting site shows mixed inflammatory cell infiltrates with eosinophils scattered among collagen bundles in an edematous dermis. Myocardial changes, which are most prominent at the papillary muscle and subendocardial region, include focal myocardial necrosis; myofibril destruction, especially at the I band; fine fatty deposits in the cardiac muscle fibers; interstitial edema; and increased cellularity, mainly lymphocytes and monocytes. Changes resemble interstitial hypoxia-induced myocarditis caused by large doses of catecholamines.

 

Treatment

Prehospital Care

Primary assessment of airway, breathing, and circulation takes precedence.

Few studies have evaluated the utility of most first aid.

The utility of negative pressure extraction devices has not been evaluated for scorpion stings.

Perform endotracheal intubation and vascular access as needed.

Emergency Department Care

Supportive care in all cases and antivenom in severe cases are used for the treatment of scorpion envenomation.

Grades of Centruroides envenomation are as follows:

  • Grade I - Local pain and/or paresthesias at the site of envenomation

  • Grade II - Pain and/or paresthesias remote from the site of the sting, in addition to local findings

  • Grade III - Either cranial nerve/autonomic dysfunction or somatic skeletal neuromuscular dysfunction, as follows:

    • Cranial nerve dysfunction - Blurred vision, roving eye movements, hypersalivation, tongue fasciculations, dysphagia, dysphonia, problems with upper airway

    • Somatic skeletal neuromuscular dysfunction - Restlessness, severe involuntary shaking or jerking of the extremities that may be mistaken for a seizure

  • Grade IV - Combined cranial nerve/autonomic dysfunction and somatic nerve dysfunction

Androctonus australis Hector Hospitalization Score is as follows (total ≥2 = Hospitalization)[31] :

  • Priapism: +3

  • Vomiting: +2

  • SBP >160: +2

  • Corticosteroid PTA: +2

  • Temperature >38ºC: +1

  • Heart rate >100 bpm: +1

Although grading and scoring systems have been developed, they are limited due to species specificity and low-degree symptoms that would lead to hospitalization or therapy.

Medical Care

Because the clinical manifestations and severity of the symptoms vary among patients, individualize management of scorpion stings. Furthermore, frequent patient monitoring allows earlier recognition of the life-threatening problems of scorpion envenomation. Treatment generally consists of moving the patient away from the scorpion and stabilizing the patient's airway and vital signs, followed by administration of antivenin and institution of symptomatic and local treatment.

Local treatment

Use ice bags to reduce pain and to slow the absorption of venom via vasoconstriction. This is most effective during the first 2 hours following the sting. Alternatively, hot water immersion has been described as a first aid treatment for scorpion bites in Australia and in Taiwan.[32, 33] A randomized controlled trial performed in Taiwan suggests that hot water immersion for Scolopendra bites is as effective as ice pack treatment in relieving pain.

Immobilize the affected part in a functional position below the level of the heart to delay venom absorption.

Calm the patient to lower the heart rate and blood pressure, thus limiting the spread of the venom.

For medical delay secondary to remoteness, consider applying a lymphatic-venous compression wrap 1 inch proximal to the sting site to reduce superficial venous and lymphatic flow of the venom but not to stop the arterial flow. Only remove this wrap when the provider is ready to administer systemic support. The drawback of this wrap is that it may intensify the local effects of the venom.

Apply a topical or local anesthetic agent to the wound to decrease paresthesia; this tends to be more effective than opiates and ice application.[34]

Administer local wound care.

Administer tetanus prophylaxis.

Administer systemic antibiotics if signs of secondary infection occur.

Administer muscle relaxants for severe muscle spasms (ie, benzodiazepines.)

Systemic treatment

Systemic treatment is instituted by directing supportive care toward the organ specifically affected by the venom.

Establish airway, breathing, and circulation (ie, ABCs) to provide adequate airway, ventilation, and perfusion.

Monitor vital signs (eg, pulse oximetry; heart rate, blood pressure, and respiratory rate monitor).

Use invasive monitoring for patients who are unstable and hemodynamic.

Administer oxygen.

Administer intravenous fluids to help prevent hypovolemia from vomiting, diarrhea, sweating, hypersalivation, and insensible water loss from a tropical environment.

Perform intubation and institute mechanical ventilation with end-tidal carbon dioxide monitoring for patients in respiratory distress.

For hyperdynamic cardiovascular changes, administration of a combination of beta-blockers with sympathetic alpha-blockers is most effective in reversing this venom-induced effect. Avoid using beta-blockers alone because this leads to an unopposed alpha-adrenergic effect. Also, nitrates can be used for hypertension and myocardial ischemia.

For hypodynamic cardiac changes, a titrated monitored fluid infusion with afterload reduction helps reduce mortality. A diuretic may be used for pulmonary edema in the absence of hypovolemia, but an afterload reducer, such as prazosin, nifedipine, nitroprusside, hydralazine, or angiotensin-converting enzyme inhibitors, is better. Inotropic medications, such as digitalis, have little effect, while dopamine aggravates the myocardial damage through catecholaminelike actions. Dobutamine may be a better choice for the inotropic effect.[35] Finally, a pressor such as norepinephrine can be used as a last resort to correct hypotension refractory to fluid therapy.

Administer atropine to counter venom-induced parasympathomimetic effects.

Other treatment

Insulin administration in scorpion envenomation animal experiments has helped the vital organs to use metabolic substrates more efficiently, thus preventing venom-induced multiorgan failure, especially cardiopulmonary failure. Unfortunately, no human studies have been conducted.

Administer barbiturates and/or a benzodiazepine continuous infusion for severe excessive motor activity. In some cases, be aware that meperidine and morphine may potentiate the venom. Also, the concurrent use of barbiturates and narcotics may add to the respiratory depression in patients who have been envenomated.

The use of steroids to decrease shock and edema is of unproven benefit.

A vaccine preparation was tried in experimental animals but was not pursued because of the need to prepare different antigens according to different geographical areas and to different species of scorpions living in the same area.

Antivenom

Antivenom is the treatment of choice after stabilization and supportive care. Because of the heterogeneity of venom composition between different scorpion species, one species' antivenom will have limited effect on another scorpion species' venom. Thus, correct scorpion species identification is a prerequisite for proper antivenom treatment.

For newer scorpion antivenom, the exact dosing has not been established as animal studies treatment amount does not translate into human studies treatment amount. In addition, the quantity to be used is determined by the patient’s clinical severity, symptom evolution, and treatment response. Unfortunately, predicting the patient’s response treatment is difficult, which makes exact antivenom dosing difficult. Furthermore, underdosing will result in limited or no effect, while overdosing increases the side effects and hypersensitivity reactions. Because the new antivenoms are highly purified immunoglobulin fragments, adverse reaction is less frequent and tends to be mild.

The antivenom significantly decreases the level of circulating unbound venom within a few hours. The persistence of symptoms after the administration of antivenom is due to the inability of the antivenom to neutralize scorpion toxins already bound to their target receptors. Thus, symptomatic and supportive treatment is needed with immunotherapy.[35]

General time guidelines for the disappearance of symptoms after antivenom administration are as follows:

  • Centruroides antivenom: Severe neurologic symptoms reverse in 15-30 min. Mild-to-moderate neurologic symptoms reverse in 45-90 min.

  • Non-Centruroides antivenom: In the first hour, local pain abates. In 6-12 hours, agitation, sweating, and hyperglycemia abate. In 6-24 hours, cardiorespiratory symptoms abate.

While an anaphylaxis reaction to the antivenom is possible, the patient is at lower risk for this than with other antivenoms for other envenomations if there is a scorpion venom—induced large release of catecholamines. Also, animal-derived antivenom increases the risk of hypersensitivity reaction compared to human monoclonal-derived antivenom. Finally, the larger the dose of antivenom, the greater the change for serum sickness.

In a prospective, randomized, double-blind study, Boyer et al compared scorpion-specific F(ab')2 antivenom (Anascorp, Centruroides [scorpion] immune F(ab)2 intravenous [equine], Instituto Bioclon) (n=8) with placebo (n=7) in children who developed neurotoxic symptoms following scorpion envenomation.[36] Neuromotor abnormalities were present in all patients at baseline, and respiratory distress was present in 20%. Beginning 2 hours after treatment, symptom resolution differed significantly in the antivenom group compared with the placebo group. Plasma venom concentrations were undetectable and cessation of the neurologic syndrome occurred within 4 hours in 100% of antivenom recipients compared with 1 placebo recipient (p=0.001).

Thus, the Boyer et al study suggests that scorpion-specific F(ab')2 antivenom successfully treated the clinical syndrome, reducing the need for concomitant sedation and reducing circulating unbound venom levels for Centruroides envenomation.[36]

For Mesobuthus tamulu envenomations, horse-derived antivenom has been developed. Natu et al compared the newer antivenom treatment versus the traditional prazosin treatment in their open label study of 81 envenomated patients and found that antivenom decreased clinical recovery time to 4.14 hours +/- 1.6 hours compared to prazosin’s clinical recovery time of 19.28 hours +/- 5.03 hours.[37]

Natu et al also found that the antivenom plus prazosin combination group had a recovery time of 3.46 hours +/- 1.1 hours but felt it was comparable to the antivenom group recovery time and recommended that the combination therapy be reserved for patients presenting with pulmonary edema with hypertension.

Bawaskar et al compared antivenom plus prazosin versus prazosin in their open label trial of 70 patients with only grade 2 envenomations (beginning of systemic involvement) and found that 91.4% of the combination treatment group had resolution of their clinical symptoms within the 10-hour mark compared to 22.9% in the prazosin treatment group.[38] Both the Natu and the Bawaskar studies suggest the utility of the new Mesobuthus tamulus antivenom for systemic symptoms envenomations.

Kumar et al found that early (< 4 h) administration of antivenom with prazosin increases the percentage of children not developing myocardial dysfunction.[39, 40]

Further inpatient care

Inpatient care is dictated by the severity of the envenomation and consists of stabilizing the patient, neutralizing the venom, providing supportive therapies, and preventing complications. Patients with grade III or grade IV Centruroides stings and other severe Buthidae envenomations should be admitted to the intensive care unit (ICU) and/or treated with antivenom.

Treat all patients with severe systemic symptoms in an intensive care unit (ICU) setting because of the unpredictability of the symptomology, the risks associated with antivenin administration, and the need for airway or blood pressure support.

Young children do worse than adults. Young children may not recover as quickly as adults after scorpion envenomation and are more likely to require observation.

Transfer

Transfer is appropriate if antivenin administration or ICU treatments are not available at the institution where the patient initially presents.

Consultations

Local poison control centers may assist in management of envenomations.

Contact the American Association of Poison Control Centers (800-222-1222) to be connected to a local poison control center.

The University of Arizona Poison and Drug Information Center (520-626-6016 from outside Arizona or 800-362-0101 from Arizona only) has special experience in Centruroides envenomation.

The Antivenom Index, published jointly by the American Association of Poison Control Centers and the American Zoo and Aquarium Association, lists the locations, amounts, and various types of antivenom stores.

Activity

Rest and immobilization of the sting site is recommended to prevent rapid absorption of the venom into the circulation.

Prevention

Protective clothing, such as shoes or gloves, may prevent some scorpion envenomations. Check shoes, gloves, clothing, and backpacks for scorpions prior to use.

Keep yards free of debris, which can serve as a place for scorpions to hide.

Make sure windows and doors fit tightly to prevent scorpions from entering the house.

Avoid walking barefoot, especially at night when scorpions are active.

Use a Wood lamp at night because the cuticle of the Centruroides species is fluorescent under ultraviolet light.

Methods of biological control of scorpions include introducing chickens, ducks, and owls to the area.

Methods of chemical control of scorpions include using organophosphates, pyrethrins, and chlorinated hydrocarbons.

Government monitoring of the scorpion public health problem is warranted.

Long-Term Monitoring

Patients displaying local nonascending reactions to the venom may be discharged after 6 hours of observation, with close follow-up. If the patient was treated with a pressure bandage, the symptoms may be delayed and inpatient observation is warranted. Patients with grade I or grade II Centruroides envenomations may be discharged. Discharge of patients with other Buthidae envenomations is more problematic because onset of systemic symptoms may be delayed up to 24 hours.

If an antivenin is administered, monitor the patient for serum sickness over next the few weeks.

Inform the patient about the possibility of persistent pain or paresthesia at the sting site.

Instruct patient regarding progression. Discuss symptoms of delayed serum sickness with patients treated with antivenom.

 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to neutralize the toxin.

Analgesia may be indicated. Exercise caution when using narcotics for a patient with an unsecured airway because respiratory depressive effects may be synergistic with some scorpion venoms. Some recommend against using narcotics to treat scorpion envenomation with signs of systemic toxicity, especially in children. Tetanus prophylaxis is recommended if the patient cannot verify current status. Prophylactic antibiotic therapy is not required. Corticosteroids have not been shown useful in treating venom toxicity. Hypertensive emergencies may require standard antihypertensive therapy. Conversely, hypotension may require fluid resuscitation and/or vasopressors.

Cardiovascular agents can be used to elevate or decrease blood pressure and increase heart rate. Vasopressors and inotropic agents may be necessary in patients who already have been adequately volume resuscitated but remain in shock. Conversely, antihypertensives may be needed in patients with sympathetic-induced hypertension. In particular, the use of the alpha-blocking agent prazosin has been used and recommended. However, most of the published evidence recommending for or against this agent has come from either retrospective observational or prospective cohort studies. Gupta et al compared dobutamine versus prazosin in children and found mortality in both groups to be equal, but the prazosin group had a quicker resolution in their pulmonary edema (28 h vs 72 h).[41] For prazosin-resistant cardiotoxic cases, a small retrospective observational study that found the addition of dobutamine to the prazosin may be beneficial.[42]

At this time, no clear evidence exists as to which agent is most beneficial in specific circumstances. Autonomic instability from scorpion envenomation may lead to rapid, dramatic fluctuations in heart rate and blood pressure. Although many agents have rapid onset, they may also have prolonged effects. Should a hypertensive patient receive a longer-acting agent they may still have medication effects if they develop subsequent hypotension. In any case, agents should be chosen with detailed knowledge of their pharmacology and understanding of the pathophysiology of scorpion venom described above. Ideally, the agents are effective, have rapid onset, can be titrated to effect, have a short half-life if discontinued, and have minimal side effects.

A total of 22 types of scorpion antivenom are listed in the American Zoo and Aquarium Association Antivenom Index. They are available for a number of different species and have varied efficacy. Antivenom use remains controversial. Many researchers report decreased morbidity, mortality, and hospital stay with its use. These researchers and clinicians believe that antivenom therapy cannot be matched by supportive care in severe Buthidae scorpion envenomation. Others suggest that adverse effects (eg, anaphylactic reactions, serum sickness) limit or contraindicate antivenom use.

Scorpion toxins are not good antigens because of small size and poor immunogenicity. They do not induce antibodies that cross-react against toxins of other scorpion species unless a 95% amino acid sequence homology exists between the 2 toxins. Thus, no universal antivenin is available.

Furthermore, the neurotoxin component of the scorpion venom tends to be the least immunogenic, resulting in the low efficiency for neurological complications. It usually is prepared from horses because they yield larger quantities. Sheep, goat, or bovine antivenins have been prepared if patient sensitivity to horse serum occurs.

One idea was to mix a batch of different scorpion antivenin together to create a universal antivenin, but this exposes the patient to unnecessary antivenin from scorpion species not from the patient's region.

Skin tests have been performed to test for allergic response with locally produced antivenins. First, dilute 0.1 mL of antivenin in a 1:10 ratio with isotonic sodium chloride solution. Second, administer 0.2 mL intradermally. A positive test result is if a wheal develops within 10 minutes. The skin test has a sensitivity of 96% and a specificity of 68%.

Until mid 2000, the antivenom for stings by the bark scorpion was manufactured in the Antivenin Production Laboratory of Arizona State University. Its use was controversial. It had been shown to produce rapid resolution of systemic symptoms but not to affect pain or paresthesias. Subsequently, many physicians recommended it in grade III and grade IV envenomations. Adverse effects included immediate and delayed hypersensitivity reactions. Initially, these reactions were rare, but they increased in frequency. This leads some physicians to prefer supportive care only, as they felt that the treatment was potentially worse than the disease. As death was rare if existent, they felt supportive care would yield similar outcomes. Currently, it is no longer being produced.

The best result occurs when antivenin is administered as early as possible (preferably within the first 2 h after the sting) and with adequate quantities to neutralize the venom (usually 50-100 times the LD50 amount). A decrease in curative effects occurs with longer sting-serotherapy delay and administration of insufficient amounts of antivenin.

In August 2011, the US Food and Drug Administration approved use of a Mexican Centruroides antivenom (Anascorp, manufactured by Instituto Bioclon for Rare Disease Therapeutics, Inc).[43]

Give steroids and antihistamines if serum sickness develops.

Antivenins

Class Summary

These agents are composed of venom-specific F(ab’)2 fragments of immunoglobulin G (IgG) that bind and neutralize venom toxins, facilitating redistribution away from target tissues and elimination from the body.

Antivenin, Centruroides (scorpion) (Anascorp)

This is a Centruroides (scorpion) immune F(ab)2 (equine) injection. it is antivenom indicated for treatment of clinical signs of scorpion envenomation. Initiate treatment as soon as possible in patients who develop clinically important signs of scorpion envenomation, including, but not limited to, loss of muscle control, roving or abnormal eye movements, slurred speech, respiratory distress, excessive salivation, frothing at the mouth, and vomiting.

Antihistamines

Class Summary

Antihistamines prevent the histamine response in sensory nerve endings and blood vessels. They are more effective in preventing a histamine response than in reversing it.

Cimetidine (Tagamet)

Cimetidine is an H2 antagonist that, when combined with an H1 type, may be useful in treating itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis that do not respond to H1-receptor antagonists alone. Use this in addition to H1 antihistamines. Other H2 antagonists are also available.

Diphenhydramine (Benadryl, Benylin, Bydramine)

Diphenhydramine is used for the symptomatic relief of allergic symptoms caused by histamine released in response to allergens.

Toxoids

Class Summary

Wounds resulting from scorpion sting are at risk of Clostridium tetani infection. A booster injection in previously immunized individuals is recommended to prevent this potentially lethal syndrome. Administer tetanus immune globulin (Hyper-Tet) to patients not immunized against C tetani products (eg, persons who have immigrated, elderly individuals).

Diphtheria-tetanus toxoid (dT)

Diphtheria-tetanus toxoid is used to induce active immunity against tetanus in selected patients. Tetanus and diphtheria toxoids are the immunizing agents of choice for most adults and children older than 7 years. Booster doses are necessary to maintain tetanus immunity throughout life because tetanus spores are ubiquitous.

In children and adults, administer it into the deltoid or midlateral thigh muscles. In infants, the preferred site of administration is the mid thigh laterally

Immune globulins

Class Summary

These agents induce passive immunity. Administer to patients not immunized against C tetani products (eg, persons who have immigrated, elderly individuals).

Tetanus immune globulin (TIG)

Tetanus immune globulin is used for passive immunization of any person with a wound that might be contaminated with tetanus spores.

Benzodiazepines

Class Summary

By increasing the action of GABA (inhibitory neurotransmitter), benzodiazepines counteract scorpion-induced excessive motor activity and nervous system excitation.

Lorazepam (Ativan)

Lorazepam is a sedative hypnotic with a short onset of effects and relatively long half-life. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, it may depress all levels of the CNS, including limbic and reticular formation.

Midazolam (Versed)

Midazolam is a short-acting benzodiazepine that can be administered in continuous infusion for severe nervous system excitation.

Barbiturates

Class Summary

Barbiturates are used to counteract scorpion-induced hyperactivity.

Pentobarbital (Nembutal)

Pentobarbital is a short-acting barbiturate with sedative and anticonvulsant properties. It is used to produce barbiturate coma for severe CNS hyperexcitation. It requires patient intubation prior to use.

Local anesthetics

Class Summary

These agents tend to be more effective than opiates to control paresthesia and pain at the sting site.

Bupivacaine (Marcaine)

Bupivacaine may reduce pain by slowing nerve impulse propagation and reducing action potential, which, in turn, prevents the initiation and conduction of nerve impulses.

Adrenergic blocking agents and vasodilators

Class Summary

Adrenergic blocking agents and vasodilators are used to counteract the scorpion-induced adrenergic cardiovascular effect.

Labetalol (Normodyne, Trandate)

Labetalol blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic receptor sites, decreasing blood pressure.

Prazosin (Minipress)

Prazosin counteracts the scorpion-induced adrenergic cardiovascular effects. It may improve pulmonary edema through vasodilatory effects.

Hydralazine (Apresoline)

Hydralazine decreases systemic resistance through direct vasodilation of arterioles.

Anticholinergics

Class Summary

Anticholinergics are used to counteract scorpion-induced cholinergic symptoms. Current recommendations are for use in treating symptomatic bradycardias. Traditionally, its use to dry venom-induced, excess, respiratory secretions has been warned against because of its potential adverse cardiopulmonary effects. It may exacerbate pulmonary edema and hypertension and may lead to a subsequent tachycardia. A recent case series has suggested relative efficacy and safety with its use in 5 pediatric patients treated for C sculpturatus sting. However, this should be considered an area in need of further study rather than a change in recommendations.

Atropine IV/IM (Atropair)

Atropine is used to increase the heart rate through vagolytic effects, causing an increase in cardiac output. It also treats bronchorrhea associated with scorpion envenomations. Atropine causes a reversible blockade of muscarinic receptors with subsequent anticholinergic effects. It has been used to reverse vagally induced symptomatic bradycardias, which may be associated with scorpion envenomation. Its use for dry secretions is debated. Atropine will not reverse the somatic or other cranial nerve symptoms.

Vasopressors/inotropics

Class Summary

Vasopressors/inotropics are used to combat hypotension refractory to intravenous fluid therapy.

Norepinephrine (Levophed)

Norepinephrine is indicated for persistent hypotension not responsive to judicious fluid loading and sodium bicarbonate.

Dobutamine (Dobutrex)

Dobutamine is a sympathomimetic amine with stronger beta than alpha effects. It increases the inotropic state with afterload reduction.

Milrinone (Primacor)

Milrinone is a positive inotropic agent and vasodilator with little chronotropic activity.

 

Questions & Answers

Overview

What is the global incidence of scorpion envenomation?

What do scorpions look like?

What are the manifestations of scorpion envenomation?

How are venomous scorpions differentiated from nonvenomous scorpions?

Which scorpions are lethal and where are they commonly found?

Where do scorpion stings commonly occur?

How do scorpions inject venom in their prey?

What is the pathophysiology of scorpion envenomation?

What are the pathophysiologic targets of scorpion venom?

What is the pathophysiology of neurotoxin in scorpion venom?

What causes scorpion envenomation?

What is a lethal dose of scorpion venom?

How much scorpion venom is released on average per sting?

What is the incidence of scorpion envenomation in the US?

What is the global incidence of scorpion envenomation?

What are the racial predilections of scorpion envenomation?

How does gender affect susceptibility to scorpion envenomation?

How does the susceptibility to scorpion envenomation vary by age?

What is the mortality rate for scorpion envenomation?

How does age and location affect mortality rates for scorpion envenomation?

What is the prognosis of scorpion envenomation?

What information about scorpion envenomation should patients receive?

Presentation

What is the focus of clinical history in patients with scorpion envenomation?

Which factors that affect the toxicity and duration of the symptoms of scorpion envenomation?

What is the duration of symptoms from scorpion envenomation?

What are the sympathetic signs of a scorpion envenomation?

What are the parasympathetic signs of a scorpion envenomation?

What are the signs and symptoms of scorpion envenomation?

What are the autonomic symptoms of scorpion envenomation?

What are the cranial nerve effects of scorpion envenomation?

What are the somatic effects of scorpion envenomation?

What are the physical findings characteristic of scorpion envenomation?

What are physical findings characteristic of scorpion envenomation in children?

How is scorpion envenomation without neurological symptoms graded?

How is scorpion envenomation with neurological symptoms graded?

What are the signs and symptoms of scorpion envenomation at the sting site?

How does the venom dose affect the clinical manifestations of scorpion envenomation?

What are the central nervous system signs of scorpion envenomation?

What are the autonomic nervous system signs of a scorpion envenomation?

What are the somatic signs of a scorpion envenomation?

What are the signs of cranial nerve involvement in scorpion envenomation?

What are the peripheral nervous system signs of scorpion envenomation?

What are the cardiac symptoms of scorpion envenomation?

What causes cardiovascular collapse in scorpion envenomation?

What are the respiratory signs of scorpion envenomation?

What are the possible allergic reactions to scorpion envenomation?

What are the GI symptoms of scorpion envenomation?

What are the genitourinary symptoms of a scorpion envenomation?

What are the hematological signs of scorpion envenomation?

What are the metabolic signs of scorpion envenomation?

How does scorpion envenomation complicate pregnancy?

Which symptoms of scorpion envenomation are predictive of hospital admission?

Which symptomatology is species specific in scorpion envenomation?

What are the complications of scorpion envenomation?

DDX

What are the differential diagnoses for Scorpion Envenomation?

Workup

What is the role of lab studies in the workup of scorpion envenomation?

What is the role of imaging studies in the workup of scorpion envenomation?

What is the role of arterial blood gas in the workup of scorpion envenomation?

Which findings on pulmonary artery catheterization are characteristic of scorpion envenomation?

What is the role of serial spirometry in the workup of scorpion envenomation?

What is the role of electrocardiography in the workup of scorpion envenomation?

Which findings on spinal tap is characteristic of scorpion envenomation?

Which histologic findings are characteristic of scorpion envenomation?

Treatment

What is included in prehospital care for patients with scorpion envenomation?

What is included in emergency department care for patients with scorpion envenomation?

What are the grades of Centruroides scorpion envenomation?

What is the Hector Hospitalization score for Androctonus australis?

How is scorpion envenomation treated?

What is included in localized treatment of scorpion envenomation?

What are the systemic treatment options for scorpion envenomation?

What are the treatments for hyperdynamic and hypodynamic cardiovascular effects of scorpion envenomation?

What is the role of insulin in the treatment of scorpion envenomation?

What is the role of barbiturates and benzodiazepine in the treatment of scorpion envenomation?

Which treatments have not proven beneficial in the treatment of scorpion envenomation?

What is the role of antivenom in the management of scorpion envenomation?

How quickly do symptoms dissipate following antivenom administration for scorpion envenomation?

What is the effectiveness of antivenom for scorpion envenomation?

What is included in inpatient care of patients with scorpion envenomation?

When is transfer needed for the treatment of scorpion envenomation?

Which medical personnel should be consulted in the management of scorpion envenomation?

What activity modifications are needed during the treatment of scorpion envenomation?

How is scorpion envenomation prevented?

What is included in long-term monitoring following treatment of scorpion envenomation?

Medications

What are the goals of drug treatment for scorpion envenomation?

Which medications are used in the management of scorpion envenomation?

What is the efficacy of antivenom in the treatment of scorpion envenomation?

How is allergy to antivenom determined prior to treatment of scorpion envenomation?

Why is bark scorpion antivenom for scorpion envenomation no longer produced?

How should antivenom be administered for the best result in the treatment of scorpion envenomation?

Which antivenom has received FDA approval for treatment of scorpion envenomation?

Which medications in the drug class Vasopressors/inotropics are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Anticholinergics are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Adrenergic blocking agents and vasodilators are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Local anesthetics are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Barbiturates are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Benzodiazepines are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Immune globulins are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Toxoids are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Antihistamines are used in the treatment of Scorpion Envenomation?

Which medications in the drug class Antivenins are used in the treatment of Scorpion Envenomation?